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Progress towards understanding anterior knee pain after total knee arthroplasty
Breugem, S.J.M.
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Breugem, S. J. M. (2014). Progress towards understanding anterior knee pain after total knee arthroplasty
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Download date: 16 Jun 2017
Chapter 2
Anterior Knee Pain after a Total
Knee Arthroplasty
What can cause this pain?
S.J.M. Breugem, D. Haverkamp
(accepted in the World Journal of Orthopedics)
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Chapter 2
Abstract
Total Knee Arthroplasty has been shown to be a successful procedure for
treating patients with osteoarthritis, and yet approximately 5-10 % of our
patients experience residual pain, especially in the anterior part of the knee.
Many theories have been proposed to explain the etiology of this Anterior
Knee Pain (AKP) but, despite improvements having been made, AKP remains
a problem. AKP can be described as retropatellar or peripatellar pain, which
limits patients in their everyday lives. Patients suffering from AKP experience
difficulty in standing up from a chair, walking up and down stairs and riding a
bicycle.
The question we asked was: “How can a ‘perfectly’ placed TKA still be painful:
what can cause this pain?”
To prevent AKP after TKA it is important to first identify the different anatomical
structures that can cause this pain. Greater attention to and understanding of
AKP should lead to significant pain relief and greater overall patient satisfaction
after TKA. This article is a review of what pain is, how nerve signalling works and
what is thought to cause Anterior Knee Pain after a Total Knee Arthroplasty.
Key words anterior knee pain, patellofemoral pain, total knee arthroplasty,
malrotation, homeostasis
Core tip: Total Knee Arthroplasty (TKA) has been shown to be a successful
procedure for treating patients with osteoarthritis, and yet approximately 5-10
% of our patients experience anterior knee pain (AKP). To prevent AKP after
TKA it is important to first identify the different anatomical structures that can
cause this pain. Greater attention to and understanding of AKP should lead
to significant pain relief and greater overall patient satisfaction after TKA.
This article is a review of what pain is, how nerve signalling works and what is
thought to cause AKP after a TKA.
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AKP after TKA: What can cause this pain?
Introduction
One of the remaining challenges in the field of Total Knee Arthroplasty (TKA)
is the elimination of Anterior Knee Pain. TKA itself has been shown to be a
successful procedure for treating patients with osteoarthritis[14], and yet a
significant proportion of the patients still experience AKP after surgery. The
symptoms of AKP after TKA can be described as retropatellar or peripatellar
pain limiting patients in their everyday lives[12]. Patients suffering from AKP
experience difficulty in standing up from a chair, walking up and down stairs,
and riding a bicycle.
In the early TKA designs the primary goal was resurfacing the medial and lateral
compartments and little attention was paid to the patellofemoral joint (PFJ)[54].
In these designs a 40% to 58% rate of patellofemoral pain was identified[18].
Insall et al[34] in 1976 hypothesized that the residual pain was most frequently
attributed to the patellar compartment. During the early years of TKA
residual AKP was often treated with either a patellectomy and/or soft tissue
realignment[34]. It would therefore, seem more appropriate to refer to Anterior
Knee Pain (AKP) rather than patellofemoral pain as the general term for pain in
the anterior part of knee. The continuing high incidence of postoperative AKP
led to the changes in the shape of the patellofemoral part of the TKA, such as
modifying the femoral trochlea and placing a patella component[34,54].
The first step in understanding AKP after TKA is to look at a healthy functioning
knee. According to the theory of Dye, “the healthy knee can be viewed as a
biologic transmission with a complex assemblage of living asymmetrical
moving parts whose purpose is to accept, transfer, and ultimately dissipate
often high loads generated at the ends of the long mechanical lever arms of
the femur, tibia, patella, and fibula”[23]. Furthermore, Dye’s refers to each knee
having a unique “envelope of function”; a potential range of activity in which it
maintains a homeostasis of all surrounding tissues[23] (Figure 1).
The potential range of activity is different for individual knees, whether
healthy, arthritic or with a knee arthroplasty. An arthritic knee can be viewed
as a transmission with worn bearings, and thus with a limited capacity to
accept and transfer loads. In other words, arthritis causes the potential range
of activity to become limited, causing pain and restrictions in daily activities
such as walking and cycling, and sometimes even pain when at rest.
2
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Chapter 2
Load
(a)
jump from 3 m
jump
from 2 m
cycling
20 minutes
walking
10 km
Frequency
Figure 1: The potential range of activity or envelope of function for a specific joint: all activities fall
within the zone of homeostasis except the jump from 3 m height (Reprinted with permission from Dye
et al[23])
The fundamental aim of knee arthroplasty or joint replacement surgery is
to restore, as far as possible, a normal functioning, pain free knee. Applying
Dye’s theory to a TKA patient gives an interesting perspective. A TKA knee can
then be viewed as a knee functioning with a combined biologic and artificial
transmission with a limited potential range of activity. The limitation is in
part due to the use of artificial products containing metals and polyethylene,
which are harder and less flexible than the original cartilage and therefore
make it unlikely that the knee will return fully to its pre-injury/pre-arthritis
state. A pain free knee with a good function can be described in Dye’s terms
as functioning in a zone of homeostasis of all knee tissues. The knee that is
structurally overloaded, and thus functioning in a zone of abnormal loading
(supraphysiological) of knee tissues is clearly no longer functioning in the
zone of homeostasis[23]. If this abnormal loading of the knee continues for long
periods of time, a TKA can ultimately fail (i.e., it enters the zone of structural
failure)[23] (Figure 2 and 3).
Although numerous design improvements have reduced the incidence of AKP,
nevertheless approximately 5%-10% of patients still experience Anterior Knee
Pain (AKP)(ranging from 0.4%-49%)[2,4,8-9,12,14-19,26,29-31,46-47,54,59,62-63,67]. Many theories
have been proposed to explain the etiology of AKP[2,4,8-9,12,14-19,26,29-31,46-47,54,59,6263,67,52]
. In sports medicine it has been observed that some patients can have
severe patellofemoral pain while their articular cartilage appears normal, and
that patients with severe patellofemoral cartilage damage can be pain free [25].
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AKP after TKA: What can cause this pain?
Even though significant knowledge exists about AKP after TKA, its etiology and
pathogenesis are still not fully understood. In this review the most important
factors related to the development of AKP after TKA are therefore analysed,
starting with how this pain signalling works and what anatomical structures can
cause this pain to occur after TKA.
2
Figure 2: The different zones of loading across the knee joint. The first zone is the zone of subphysiological
underloading, the second is the preferred zone of tissue homeostasis, the third is the zone of
supraphysiological overloading and the fourth is the zone of structural failure (Reprinted with
permission from Dye et al[23])
Figure 3: A: Arthritis causes the potential range of activity (envelope of function) to become limited,
causing pain and restrictions in daily activities such as walking and cycling. The dotted line is the original
zone of homeostasis for this specific knee; B: The postoperative situation where Total Knee Arthroplasty
placement increases the potential range of activity but does not return it to the original range of activity.
(Reprinted with permission from Dye et al[23]).
Pathophysiology and Etiology of Pain
Pain is a normal manifestation of everyday life and serves as a protective
mechanism for the body, causing the individual to react to try to eliminate the
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Chapter 2
pain stimulus[12,22]. However, excessive pain after a TKA can diminish or hinder
quality of life [16,59,62],[22]. This form of pain typically originates in the peripheral
nervous system (PNS)[22].
The PNS consists of all the nerves outside of the brain and the spinal cord[22,13].
It is made up of bundles of axons which are enclosed by connective tissue to
maintain the continuity, nourish and protect the axon[13]. Each axon in the PNS
can be surrounded by a myelin sheath, called a Schwann cell sheath, and these
two together form a nerve fibre[13]. An axon can be myelinated once it reaches
a thickness of one or two micro metre[13]. The difference between a myelinated
and non-myelinated nerve fibre is the conduction velocity (myelinated is faster)
[13]
. Nerve fibres can therefore be classified into different types depending on
their diameter and conducting velocity[13].
When nerve fibres transmit information from sensory receptors to the central
nervous system (CNS) they are called afferent nerves[13]. Afferent nerves are
triggered by specialized neural structures called sensory receptors[13]. These
receptors are sensitive to a specific form of physical energy[13]. In the joint these
are called joint receptors or mechanoreceptors and can be divided into four
basic categories: Ruffini endings (stretch), Pacinian corpuscles (pressure and
pain), Golgi tendon organ-like endings and Free Nerve Endings (FNE)[12-13].
Pain occurs when tissues are being compressed, damaged or irritated[12]. The
perception of pain appears to be activated by pain-specific sensory receptors
called nociceptors in a process called nociception [49]. FNE, especially type IV
FNEs detect touch, pressure, pain, heat and cold[12].
These FNEs primarily form the basis of the nociceptive system by sending
signals to the spinal cord and CNS on pain and inflammation [12,49]. Under
normal circumstances FNEs remain inactive, but they become active when
subjected to abnormal mechanical deformation, thermal stimuli or special
chemical agents[12,49]. Pain signals are transmitted to the CNS by a fast or a slow
pathway[12]. Fast pain can be triggered by mechanical and thermal stimuli, but
slow pain can be caused by mechanical and thermal stimuli and by chemical
agents[12]. Fast pain is transmitted through A fibres (also called A delta fibres,
they are myelinated) at velocities estimated to be between 6m and 100 m
per second[12-13]. This is often experienced as a sharp, acute or electric pain[12].
The slow pain is transmitted through C fibres (unmyelinated) with velocities
between 0.5 m and 2 m per second and is often described as burning, aching or
chronic pain[12-13]. This type of pain is normally present with tissue destruction
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AKP after TKA: What can cause this pain?
. Slow pain can occur in the skin and deep tissues whereas fast pain is not felt
in the deeper structures[12].
Chemical substances, as mentioned, play an important role in stimulating
the slow type of pain[12]. Chemicals that excite pain include histamine (also
causes itching), serotonin and bradykinin[12,49]. Bradykinin acts via G-proteinlinked receptors to produce a range of proinflammatory effects including
vasodilatation and edema[12,49]. Prostaglandins and Substance P (SP) enhance
the sensitivity of nociceptors but do not directly excite them[12,49]. SP can function
as a vasodilator and therefore can produce inflammation[12]. Substance P (SP)
is a neuropeptide that can function as a neurotransmitter and is detected and
isolated in the lateral retinaculum, the infrapatellar fat pad, synovial membrane,
periosteum and subchondral bone of patellae affected with degenerative
disease[12,65]. Nerve fibres immunoreactive for SP are not observed in the intact
articular cartilage and are present in degenerative erosion of the patella[12].
Examination of subchondral bone, however, shows the presence of SP positive
nerve fibres in a degenerative joint.
The problem with pain receptors is that, unlike smell or taste for example,
they adapt very little and sometimes not at all[12]. The continuous excitation of
nociceptors, therefore, tends to lead to a chronic aching pain[12]. This increase in
sensitivity of the nociceptors is called hyperalgesia[12].
Having looked at how nerves transmit pain, the next step is to focus on which
nerves are responsible for different parts of the knee joint. The innervation
of the knee joint follows Hilton’s law, meaning that all of the motor efferent
nerves carry afferent branches from the knee capsule[32,36]. The innervation
of the knee joint can be divided into two groups; a posterior and an anterior
group[32,36]. The posterior group is made up of branches of the tibial nerve
and a terminal branch of the obturator nerve. If necessary, signals from the
posterior capsule and cruciate ligaments are transmitted to the CNS[32,36]. The
anterior group consists of branches of the femoral, common peroneal and
saphenous nerves[32,36]. The femoral nerve divides into the vastus muscles and
the anterior medial joint capsule. The saphenous nerve innervates the anterior
medial capsule and some sensory branches to the patellar tendon[32,36]. The
medial side of the patella is innervated by the nerves of the vastus medialis
muscle[12]. The lateral part of the knee is innervated by the nerves of the biceps
femoris muscle and the vastus lateralis muscle[12].
[12]
2
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Chapter 2
The knee is a hinge type of joint and in the Total Knee Arthroplasty (TKA) is
made up of the articulations between the femoral and tibial components and
between the patella and the patellar surface of the femur, the patellofemoral
joint (PFJ). The femur component (metal alloy) articulates with a Polyethylene
surface either on a tibial base plate (metal alloy) or a total Polyethylene tibial
component. A hinge joint mainly allows for motion in one plane and only slight
side to side motion is possible. The femur and tibia are connected together
by strong collateral ligaments and depending on the arthroplasty used,
sometimes a posterior cruciate ligament.
The complexity of patellofemoral joint and the high number of pain transmittors
are of relevance to the issue of whether or not to resurface the patella, which is
an area of ongoing controversy in the field of TKA[2,14,18-19,30,54,64,67,11]. If the patella is
resurfaced, the articular cartilage is removed and substituted with a polyethylene
component. Alternatively, if needed, the patella can be reshaped (denervation,
a partial resection of the lateral facet, removal of osteophytes or a combination
of the above mentioned). The complexity of the PFJ means it is not only the
articulation of the patella on the femoral groove of the femur component (metal
alloy). Several muscle as well as ligament forces act on the patella to provide
stability and a proper patellar tracking. The patella allows for multidirectional
movement, especially cranial and caudal, but it also tilts and even rotates. There
are, therefore, numerous points of contact between the undersurface of the
patella and the femur component. The PFJ also depends on the synovial plica,
infrapatellar fat pad, tendons, retinacula and the capsule[12,25]. The PFJ appears to
be very sensitive to pain due to the high number of FNEs in different structures[12].
The highest numbers are found in the quadriceps muscles, with significant
numbers also in the retinacula, patellar tendon and synovium[12,25]. Intact hyaline
cartilage is completely free of nerve fibres[12,65]. Therefore intact aneural cartilage
cannot be a source of pain[12,25]. Dye had an arthroscopic palpation of his patellar
cartilage lesion done on his own knee. The operation was performed without
intraarticular analgesia. Dye reported experiencing no pain when the patellar
cartilage lesion was palpated[25]. However, he did experience severe pain when
the synovial plica, infrapatellar fat pad, tendons, retinacula and the capsule were
palpated[25].
Regeneration of Nerves
After looking at how pain signalling works, the interesting next question for
clinicians is: how can these findings be translated into practical daily patient
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AKP after TKA: What can cause this pain?
care? With the skin incision in a TKA, nerves are surgically cut, and axons are
injured or damaged[10]. The neurons can regenerate a new axon in a process
called chromatolysis[10]. The process starts with exudation, cell proliferation
and then collagen synthesis[13]. First the gap is filled with blood corpuscles
and macrophages and a fibrin clot is formed[13]. This results into an ingrowth
of capillaries and fibroblasts. This ingrowth only develops in the proximal
stump of the damaged axon by forming sprouts, as the distal part of the axon
dies[22,10]. These sprouts grow along the path of the original nerve, if this route
is still available[10]. In the distal stump the Schwann cells of the nerves not only
survive the wallerian degeneration, but also proliferate and form rows along
the course previously taken by the axons[10]. These Schwann cells form nerve
growth factor, which attracts the nerve fibres to grow back across the surgical
cut[22]. The rate of regeneration is slow and is approximately 1 mm per day in
the knee[10,13]. When peripheral nerve regeneration gets blocked in the scar
tissue, a neuroma can be formed[13,22].
Another way pain might be transmitted is when nerves around the knee are
compressed. The nerve, a soft structure, can be compressed between bone,
ligaments or due to swelling (hematoma)[22], but also by a knee arthroplasty or
the scar tissue that is formed after a TKA. Dellon describes how, when a nerve is
compressed, blood flow to the nerve is reduced [22]. When a nerve does not get
enough oxygen, it stops conducting normal signals to the CNS[22]. This can be
felt as a “buzzing” or “tingling”feeling [22].
2
Clinical Implications
Assuming that the incapacitating AKP is caused by the activation of FNE, the
main interest of this study is to know how they become active and whether
this is due to an abnormal mechanical deformation, thermal stimuli or special
chemical agent[12,49]. It is known that the structures in and around the PFJ are
very sensitive to pain, being full of nociceptors[12,49]. The synovium, lateral
retinaculum, infrapatellar fat pad, periosteum and subchondral bone of
patellae affected with degenerative disease are all richly supplied with type IVa
FNEs and fibres containing Substance P[12].
A key aim of this study was to identify literature evaluating the different
determinants of AKP after a TKA was found [1,4,8,11-12,16-17,22,24-26, 31,37,42,52-53,56,62-63,65]. The
articles reviewed confirm this study’s hypothesis that anything that alters the
patellofemoral joint (PFJ) mechanics can activate these FNEs and thus induce AKP
after TKA[62]. It can further be hypothesised that the nociceptive system can be
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Chapter 2
activated by several factors, either alone or in combination: Hoffa impingement,
peripatellar synovitis, increased osseous pressure and mechanical changes that
alter the PFJ in an abnormal way.
The influence of patient characteristics focussing on age, gender and BMI does not
seem to be predictive of AKP after TKA[4,16,57,62,64,67]. The influence of preoperative
AKP does not seem to be predictive in relation to postoperative AKP[4,16,57,62,67].
Some researchers investigated the influence of walking on AKP after TKA. A
higher knee extension moment in the early midstance phase of walking causes
higher forces on the PFJ and consequently a higher frequency and severity of AKP
after TKA[57]. Interestingly, the patients that modify and decrease the PFJ loading
had less or no AKP[57]. Muscle balance also has an influence on AKP, for instance
the preoperative weakness of the vastus medialis muscle was seen to lead to
increased activation of the vastus lateralis, and the ensuing lateral maltracking of
the patella can lead to AKP after TKA[52,20]. Weakness of the hip adductors was also
seen to lead to a dynamic valgus and thus to lateral patella maltracking, which
therefore makes it a contributor to AKP after TKA[52].
Moving on to focus on the influence of the knee design, Mahoney et al
suggested that the design of the specific TKA can have an influence on PFJ
loading[44]. They studied which designs were able to change the posterior
flexion extension axis, thereby lengthening the extensor mechanism moment
arm, which could decrease the quadriceps’ muscle force and reduce the PFJ
forces[44]. The importance of trochlear design was emphasised by Popovic, who
found a high number of patients experiencing pain due to an inappropriate
trochlear design[53]. Some other researchers have suggested that the posterior
stabilized knees have less AKP compared to the cruciate retaining designs, but
a recent meta-analysis could not prove this difference (6% AKP in both groups)
[40]
. Breugem et al[16-17] performed two studies that specifically evaluated
whether the mobile bearing knee could reduce AKP compared to the fixed
bearing knee. In the short-term follow-up study less AKP in the mobile bearing
knees compared to the fixed knees[16] was observed, which seemed to suggest
that the mobile bearing knee did have an influence on AKP [16]. Kim et al
reported less pain in the mobile bearing group compared to a fixed bearing
group at a mean follow-up of 2.6 years[38]. Wohlrab et al found a difference
in pain scores at three months favouring the mobile bearing, but found no
difference after three and five years[66]. In the 6 to 10 year (median 7.9 years)
follow-up study the mobile bearing knees did not sustain the difference in AKP
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AKP after TKA: What can cause this pain?
that had been found in the short-term study[16-17]. These results are comparable
to the findings of other systematic reviews and/or meta-analysis, most of
which have not shown an advantage of using a mobile bearing[1,7,58,62,61,60].
Based on these results combined with a recent meta-analysis showing less AKP
in the mobile bearing TKA, it seems that the debate can be reopened as to
whether the mobile bearing TKA is part of the solution to AKP[41]. Aglietti et
al[1] suggested that the performance of a mobile bearing knee might decline
over time. Yet, even if this difference is only relevant in the short term, it would
still seem advantageous to use a mobile bearing TKA for the benefit of patients
that experience less pain in this period. The reason why the mobile bearing TKA
seems to make a difference in AKP, could be due to the femur component being
highly congruent to the PE bearing this in combination with the self alignment
ability of the PE bearing and the fixed tibial base plate, in a knee that is well
balanced in flexion and extension thus unloading the PFJ.
The influence of placement of the TKA is another issue. The PFJ loading is
influenced both by changes in the joint line height and by selecting a femoral
component that is too large[42,35]. Tibia-femoral instability, due to inappropriate
placement or other causes, leads to increased pressure on the PFJ, especially
in flexion[50]. However, perhaps the most important aspect of placement is
the influence of malrotation after TKA[4,8,11,31,33,48,55]. Berger et al[8] reported
that combined component internal rotation is associated with lateral tracking
followed by patellar tilting and potential patellar subluxation. Dislocation and
component failure were reported when severe malrotation was present[8].
Barrack et al[4] studied the influence of malrotation on AKP and found a
combined internal rotation had a relative risk of AKP which was five times
higher than cases without combined component internal rotation. It is thought
that a femoral component placed in internal rotation shifts and tilts the patella
medially and this can have a negative influence on the PFJ[4,8,31,33]. This could be
an important reason to explain why secondary resurfacing of the patella does
not always solve AKP after TKA[11,45].
Without doubt the most studied aspect of AKP has been the influence of the
patella, especially in relation to resurfacing[2-3,11,19,45,54,64,67,51,28]. Many studies have
focused on patella resurfacing, some demonstrating no difference[18-19,62], some
showing better results after resurfacing [14,30,54,64,67], and others advising against
resurfacing[2,45,68]. It is known that simply resurfacing the patella is not a universal
solution for AKP, although it may solve the problem in selected cases [2,18-19,29,45,54].
2
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A meta analysis of 7 high quality studies showed no advantage for resurfacing
the patella with regard to AKP[28]. Interesting publications from the Oxford group
show that full thickness cartilage damage of the PFJ is not a contraindication for
the placement of the medial Oxford mobile bearing knee arthroplasty, since this
does not seem to influence the outcome or the revision rate[5-6]. It is still not clear
why in a mobile bearing uni compartmental knee, PFJ arthritis does not seem
to play an important role, whereas in a TKA it is a recurring debate. Maybe the
influence of the intact anterior cruciate ligament (propriocepsis) is part of the AKP
solution. Future research will hopefully provide new insights to these questions.
Finally, although soft tissue irritation is often related to malalignment, the
mechanical cause cannot always be defined. Therefore, it may be that soft
tissue problems play a significant role in AKP after TKA. Synovial impingement
after TKA can play an important role in postoperative pain[21]. Two studies
evaluated the influence of denervation of the patella and Van Jonbergen
found a difference in favour of circumpatellar electrocautery denervation[63].
One study found a lower prevalence of AKP due to the resection of Hoffa’s
fat pad[43]. Other factors contributing to AKP have been proposed; wear[59],
referred pain[59,62], patella height[42,67], patellar thickness[27,39] and patella baja
(pseudobaja), but these studies could not demonstrate a correlation with AKP
after TKA. This is often more a lack of power than proof.
Applying Dye’s theory to patients with AKP after TKA provides useful insights
(Figure 1). The zone of homeostasis can then be seen as a zone without
AKP. The zone of supraphysiological “overload” can be seen as the zone for
abnormal loading of the PFJ and therefore a cause of AKP after TKA[23]. A good
example of this is the relationship between malrotation and the severity of
experienced AKP [4]. If the components of the TKA are malrotated, the knee
tissues are overloaded and thus clearly functioning in a zone of abnormal
loading rather than in the zone of homeostasis[23]. If this abnormal loading of
the knee continues for long periods of time, a TKA can ultimately fail (i.e., it
enters the zone of structural failure) [23]. As mentioned by Berger et al[8], slightly
combined component internal rotation is associated with lateral tracking of
the patella followed by tilting and potential patellar subluxation and the knee
is thus functioning in the zone of abnormal loading, which could lead to AKP
after TKA. Dislocation and component failure were reported when severe
malrotation of the components was present and thus the knee was functioning
in the zone of structural failure[8].
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AKP after TKA: What can cause this pain?
If AKP is present after TKA placement, it is interesting to find out if it is possible
to bring the knee back into a zone of homeostasis, and if this can influence the
AKP. This can sometimes be achieved by conservative measures, for example in
the study by Smith et al[57], where patients that were able to learn how to walk
in a different way could reduce or even had no AKP, compared to patients who
could not learn how. Other corrective measures include muscle-training (the
quadriceps/hamstrings but also the hip and trunk muscles, therefore avoiding
a dynamic valgus[20,52]), medication (painkillers), taping of the patella, using
inlays or avoiding certain activities. If structural mechanical causes are present,
revision surgery may be indicated, but caution is advised within the first 12
months. This review will not focus on operative treatment options, as these are
areas for separate review.
2
Conclusion
It can be concluded that anterior knee pain after TKA can be seen as the
presenting symptom of a multifactorial problem. It is known that the
nociceptive system is being activated by abnormal mechanical deformation,
thermal stimuli or special chemical agents. The pain is caused by soft tissues
(i.e., retinaculum, infrapatellar fat pad and the synovial membrane) being
overloaded and/or due to impingement; for example due to malrotation of
the components, overstuffing of PFJ, instability of the PFJ or a combination.
Simply changing to a mobile bearing, releasing the retinacula or resurfacing
the patella does not seem to be a universal solution. A perfect placement of a
well-designed TKA can minimize AKP, however it cannot be concluded that it
will prevent AKP, due to the large number of different factors playing a role in
the origin of AKP. It is suggested that clinicians determine the specific envelope
of function or zone of tissue homeostasis for TKA patients. Future research
should focus on making further progress towards understanding the complex
interaction of factors causing AKP in order to find a solution to prevent and
eliminate it. The recommendation of this study is that the main focus should
be on determining the correct placement and maybe incorporating the ACL (if
present) in TKA placement.
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